Excessive sweating can lead to significant discomfort, both physical and emotional.
Hyperhidrosis is a medical condition in which a person sweats excessively and unpredictably. When excessive sweating affects the hands, feet, and armpits, it's called primary or focal hyperhidrosis. Primary hyperhidrosis affects approximately 2-3% of the population, yet less than 40% of patients with this condition seek medical advice. In the majority of primary hyperhidrosis cases, no cause can be found. The most prevalent form of hyperhidrosis is hyperhidrosis palmoplantaris characterized by excessive sweating of palms, soles and axillae.
If the excessive sweating occurs as a result of another medical condition, it is called secondary hyperhidrosis. The sweating may be generalized (i.e. all over the body), or it may be in a restricted area.
Prevention of excessive sweating can include Botulinum toxin administrated through injections or iontophoresis as well as antiperspirants containing aluminum chloride hexahydrate which plug the sweat ducts and may cause skin irritation. Medical treatments include anticholinergics drugs, such as glycopyrrolate, and tricyclic antidepressants. Both glycopyrrolate and tricyclic antidepressants inhibits acetylcholine on its muscarinic receptors with anticholinergic side effects such as blurred vision, constipation, dry mouth, dizziness, headache, impotence and problems with urination. Excessive sweating may also be treated by surgery and sympathetic denervation.
Inositol 1,4,5-trisphosphate receptor Type 2 (ITPR2) is an intracellular Ca2+ release channel that is expressed in many tissues. In mammalians, at least three forms of ITPR are identified assigned type 1, 2 and 3 respectively (Yule, 2010). The ITPR2 channel is a homotetrameric or a heterotetrameric structure with three functional domains; a transmembrane domain containing the Ca2+-channel pore close to the COOH-terminus, the amino-terminal IP3 binding domain, and a large cytosolic domain that connects the Ca2+ channel with the IP3-binding region. With the exception of the short transmembrane domain containing the Ca2+ pore, the major part of the ITPR2 is exposed to the cytoplasm and is a target for several accessory proteins as well as kinases.
No specific human phenotype has been reported as associated with down-regulation of, or mutations in any of the three ITPR2 genes. Furthermore, mice with a targeted disruption of ITPR2 show no abnormal phenotype (Futatsugi, 2005). However, a mouse model with deletion of both the type 2 (ITPR2) and the type 3 (ITPR3) receptor genes show exocrine dysfunction of the salivary and the pancreatic glands (Futatsugi, 2005).